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Left Anterior Fascicular Block

Sun, 09/28/2014 - 23:39 -- Dawn

This ECG provides an example of LEFT ANTERIOR FASCICULAR BLOCK (LAFB).  It is from an elderly woman for whom we have no other history.

The conduction system below the AV node consists of the Bundle of His, the left bundle branch, and the right bundle branch.  While there is some variation among individuals, most of us have two main fascicles, or branches, of the left bundle.  The ANTERIOR-SUPERIOR fascicle carries the electrical impulse to the anterior wall of the left ventricle, and the POSTERIOR - INFERIOR fascicle carries the impulse to the inferior area of the left ventricle.

Blocks can occur at any level in the conduction system, including left bundle branch block, right bundle branch block, left anterior fascicular block, left posterior block, and bi-fascicular blocks. LAFB can have many causes, including myocardial infarction, cardiomyopathies, fibrosis of the cartilagenous ring, and aortic valve disease.  Left anterior fascicular block is much more common than left posterior fascicular block. Both are also called hemiblocks.

When LAFB is present, the initial septal depolarization forces are still left to right, providing a small initial q wave in Lead I and a small r wave in Lead III.  After septal depolarization is complete, the activation vector moves inferiorly and to the right as the electrical wavefront moves through the left posterior hemifascicle and right bundle branch. The impulse finally makes its way to the left and superiorly via slow conduction through myocardium normally depolarized by the left anterior hemifascicle, which is blocked.  It is because the terminal left ventricular activation moves upward and toward the left that the  inferior leads have negative deflections.

The diagnostic criteria for LAFB are:  LEFT AXIS DEVIATION (QRS axis between -45 degrees and -90 degrees); qR pattern in Lead I; rS pattern in Lead III; delayed activation time evident in Lead aVL - the time from onset of the QRS to the peak of the R wave is 45 ms or more. (This example barely makes that criteria); QRS duration normal or slightly wide, but not 120 ms or more (unless there is also RBBB).  LAFB also causes poor R wave progression in the precordial leads, with late transition and S wave present in V6.

Before deciding on a diagnosis of LAFB, you must rule out previous or acute INFERIOR WALL M.I.  The pathological Q waves that can occur with necrosis can cause a left axis deviation in the frontal plane.  The presence of a small r wave in Lead III rules out pathological Q wave in that lead.  If any fascicular block (hemiblock or bundle branch block) occurs during the course of an M.I., the patient should be watched carefully for progression of the block.  Be prepared to pace if necessary in that situation. 

Thanks to our Consulting Expert, Dr. Ken Grauer, for his editing assistance.

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Comments

ekgpress@mac.com's picture
 
     Dawn's ECG for today addresses the controversial topic of LAHB (Left Anterior HemiBlock). Having observed marked differences in the manner in which different practicing cardiologists interpret LAHB - I long ago developed a simplified approach to the topic that in my experience works as well as more complex criteria - yet enables ready diagnosis of LAHB within seconds. My system differs a bit from Dawn's description (as it differs from other textbook descriptions) - but I believe my simplified system works as well as anything else I've seen - and it makes ECG interpretation far easier.
  • The problem I have found with requiring a specific QRS morphology pattern in the limb leads for diagnosis of LAHB - is that other conditions may influence what you see in other leads without negating the presence of underlying LAHB. This may happen not only with inferior infarction - but with ventricular enlargement, cardiomyopathy, RBBB and simple normal variation which may or may not result in small normal septal q waves. Cardiologists do not uniformly agree on the amount of left axis deviation needed to satisfy criteria for LAHB. In actually - they can't, since presence of "other conditions" may alter the "required" amount of axis deviation. Add to this the natural tendency with aging (and aging of the conduction system) for the axis to gradually shift leftward (not necessarily due to a specific conduction 'block' ) - and it becomes apparent how difficult requiring specific QRS morphologic criteria for LAHB may be.
  • For practical purposes - the presence of a "pathologic" left axis (ie, a mean QRS axis more negative than -30 degrees) - signals development of LAHB. This is EASY to recognize. Assuming the heart lies in the left side of the chest cavity (ie, net QRS deflection in lead I is positive) - IF the net QRS deflection in lead II (which is situated at +60 degrees) is more negative than positive - then the axis is MORE than 90 degrees away from lead II - or more negative than - 30 degrees.
  • Look at the tracing in this case. We can tell in seconds that there is LAD (Left Axis Deviation) - because the net QRS deflection is positive in lead I (at 0 degrees) and negative in lead aVF (at +90 degrees). To then determine IF the amount of LAD is "pathologic" - just look at lead II. If lead II was exactly isoelectric (ie, equal parts positive and negative) - then the axis would be precisely 90 degrees away - or at - 30 degrees. But since in the tracing shown here lead II is obviously more negative than positive - this means that the mean axis is clearly more negative than -30 degrees - or equivalent (for practical purpsoses) to LAHB. Total time figuring this out = less than 5 seconds, with a result that is as accurate as any obtained by more complex criteria.
  • Presence of competing conditions (ie, simultaneous inferior infarction and/or RBBB) complicate diagnosis of LAHB no matter what criteria you select. While presence of LAHB may negate the Q wave you'd normally see in lead III with inferior MI - it should NOT negate development of a Q wave in lead II. Suspicion of concomitant inferior MI + LAHB may also be made when you see a fragmented complex in the inferior leads in association with marked LAD.
  • With RBBB - the terminal delay of this conduction defect should not negate marked negativity of the earlier portion of the QRS in lead II when LAHB is also present.
P.S. Note "poor R wave progression" in the tracing here. This is NOT due to anterior infarction. Because the left anterior hemifascicle lies slightly in front of (ie, anterior to) the posterior hemifascicle - when there is LAHB, initial forces may be relatively directed posteriorly - with result that r wave progression is reduced. LAHB may also be responsible for persistent R waves seen in this case.

BOTTOM LINE: For practical purposes - LAHB is present when there is "pathologic" LAD. This can be determined in seconds. Assuming net QRS deflection in lead I is positive - there is LAHB if net QRS deflection in lead II is decidedly more negative than positive.
  • NOTE: For review of my simplified approach to ECG diagnosis of LAHB in the context of rapid determination of Axis - Please check out my ECG Basic Concepts-3 ( = ECG Blog #90). Figures 11-thru-15 deal specifically with ECG diagnosis of LAHB.
 

Ken Grauer, MD  www.kg-ekgpress.com   [email protected] 

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